We intend to continue our studies in the arthritis model, induced by immunization of rats with cartilage collagen, as well as our clinical investigations. By antigen-presentation techniques, we hope to gain additional insights into the role of T and B cells in the rat arthritis. Neuroendocrine studies may elucidate the mechanism(s) by which psychological stress can abrogate the development of arthritis in rats immunized with collagen. Pathology studies, using transmission and scanning electron microscopy, as well as immunofluorescence, should determine the sequence of intrasynovial events following injection of type II collagen. As a further correlate to our human studies, the role of autoimmune responses to homologous type III collagen in the rat model will be explored. The suitability of the model to evaluate pharmacologic agents with antirheumatic effects in humans will be addressed. We will also determine whether autoimmune responses to collagen are specific for adult rheumatoid arthritis or are features shared with other chronic proliferative synovitides, such as psoriatic arthritis or juvenile rheumatoid arthritis.